The phrase "activation questions" is correct and usable in written English.
It can be used in contexts related to education, training, or engagement strategies where questions are designed to stimulate thought or discussion.
Example: "To encourage participation, we will start the session with some activation questions to get everyone thinking."
Alternatives: "engagement questions" or "stimulus questions".
Despite fast progress in the investigation of molecular mechanisms concerning contacts between receptor and G-protein [18], [19], [22] or mechanisms of G-protein activation, fundamental questions regarding these processes are still open such as: How and where the G-protein selectivity of GPCRs is determined?
Despite the fact that inspiring progress has been achieved in miRNA-mediated gene activation, many questions remain to be further elucidated.
Patients assessed chronic illness care (PACIC) with a 20-item questionnaire comprising five pre-defined subscales: patient activation (3 questions), delivery-system/practice design (3), goal setting/tailoring (5), problem solving/contextual (4), and follow-up/coordination (5).
8 To expand this mode of activation, we questioned whether this methodology could be used to access functionalized pyridines.
Whether receptor dimerization is sufficient for activation was questioned in the past [ 33], and several studies challenged the model of purely association driven activation.
Randomized controlled trials have demonstrated that interventions to train patients to assume more active involvement in their care and to ask more appropriate and relevant questions ("activation") can improve patients' outcomes[ 25, 26].
Moreover, the differences in rodent versus human C-cell biology with regard to responsivity to GLP-1R activation raise important questions about the suitability of mice and rats as models for understanding the effects of GLP-1R agonists on human C-cells.
Pharmacological Sirt1 activation has been questioned since the in vitro activator resveratrol failed to stimulate deacetylation of several physiological substrates.
This may be a result of cell activation, but the question remains as to why the increased numbers of activated T cells in HIV infected individuals fail to clear pathogens and are ineffectual in their actions.
This apparent redundancy in FLO11 activation raises the question: Why are the two pathways retained?
